MMG 409 Exam 3 – Flashcards
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| Life depends on the ability of cells to grow, copy their genetic information, and ____ pass that information onto the next generation. |
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| Accurately |
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| What is the name of the phase that happens when the cell has left the cell cycle? |
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| G0 |
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| Why are checkpoints in the cell cycle important? |
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| 1. Allows the cell to monitor its own progress 2. Allows the controller to respond to extracellular signals from the environment and from other cells. |
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| Once the cell is past the checkpoint... |
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| it cannot pause the cell cycle. The cell is committed to completing the subsequent step. |
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| What does cdc stand for? |
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| Cell Division Cycle mutants |
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| One type of mutant phenotype involves an inactivation of some protein involved in activating or pushing the cell cycle forward. What does that mean? |
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| That you have basically blocked an activator. Meaning that the cell can no longer proceed through the cell cycle. |
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| What kinds of mutants divide early, skipping a normal control point? |
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| Wee mutants |
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| Wee mutants are expected to be deficient in a product that normally ____ passage through a size checkpoint. |
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| inhibits |
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| How do you identify the mutated gene that is responsible for the observed phenotype? |
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| add back wild type genes, until you find the one that fixes the mutation |
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| What are the two ways passage through the cell cycle is controlled by? |
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| Protein phosphorylation (CDKs) and Protein Degradation (Ubiquitin-protein ligases (adding tags)) |
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| The activity of Anaphase-promoting complex (APC/C)is important in pushing the cell through which checkpoint? |
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| Metaphase Checkpoint |
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| What is the heart of the cell cycle control system? |
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| Cyclin-Dependent Kinases (CDKs) |
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| ____ of these kinases (CDKs) rise and fall as the cell progresses through the cycle. |
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| Activity |
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| Kinase activity is dependent on presence of ____ |
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| Cyclin |
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| What are the 3 main classes of cyclins? |
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| G1, S-phase, and Mitotic cyclins |
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| Activity of the CDK is regulated by |
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| 1. Cyclin Binding 2. Phosphorylation (2 key ones) |
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| What greatly increases the affinity for protein substrates? |
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| phosphorylation |
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| What is important in control of M-CDK activity, and is caused by the addition of phosphates(2) in the roof of the active site (inhibits activity)? |
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| Inhibitory Phosphorylation |
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| What removes inhibitory phosphates like Wee1? |
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| Cdc25 |
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| CDK activity can be suppressed by? |
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| The binding of CDK inhibitor proteins(CKIs) |
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| CKIs are primarily used in controlling ___ and ____ CDKs |
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| G1 and S-phase |
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| When a CKI binds to a CDK what does it do? |
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| Rearranges structure of the CDK active site and holds the CDK inactive until needed |
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| What are the two distinct enzyme complexes crucial for cell cycle control? And they are both what? |
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| 1. APC/C (Anaphase-promoting complex) 2. SCF (S-phase Controlling Factor) Ubiquitin Ligases |
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| Enzyme complexes can tag proteins with ____. Which targets the protein for destruction in the ____. |
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| Ubiquitin, proteasome |
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| What is responsible for ubiquitylation and destruction of G1/S-cyclins and certain CKI proteins that control S-phase initiation? |
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| SCF |
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| What is important in M-phase. Responsible for ubiquitiylation and proteolysis of M-cyclins and other regulators of mitosis? |
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| APC/C |
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| Entry into the M-phase requires this crucial event. |
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| The activation of Cdc25 which removes the inhibitory phosphate, and the inactivation of Wee1 (kinase) |
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| Cdc25 is activated by phosphorylation via ___ protien kinase. |
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| 2 |
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| Wee 1 is ____ by phosphorylation. |
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| inactivated |
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| What the family of proteins required for normal chromosome segregation? |
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| SMC proteins (structural maintenance of chromosomes) |
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| What are the multiprotein complex, overlap with SMC members. ITs phosphorylation is required for condensing activity? |
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| Condensin |
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| What holds sister chromatids together? |
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| Cohesins |
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| When are cohesions loaded on? |
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| G1 |
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| In the APC/C what does ubiquitin ligase do? |
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| Inactivates protein complexes (cohesins) that connect sister chromatids at metaphase Also degrades the cohesins to permit the onset of anaphase |
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| Once sister chromatids are separated ____ is activated. |
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| Cdh1 |
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| Cdh1 is teh specificity factor directs the APC/C to the ___ ___. Cell can begin to ___ mitosis. |
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| Mitotic cyclins, exit |
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| G1 is a state of stable CDK ___ |
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| Inactivity |
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| Where is the function of S-CDK most important? |
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| in DNA replication |
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| If a cell in S-phase were fused with a cell in G1.... |
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| the G1 nucleus would immediately enter S-phase, the S-phase nucleus continues DNA replication |
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| If a cell in S-phase were fused with a cell in G2.... |
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| The G2 nucleus, would stay in G2 , the S-phase nucleus would stay in S-phase |
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| What are the two sensors in the G2 checkpoint? |
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| ATM and ATR (kinases) |
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| How is ATM activated? |
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| By recognizing double strand breaks |
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| How is ATR activated? |
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| By single stranded or unreplicated DNA |
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| ____ are extracellular structures composed of chromatin and granule proteins that bind and kill microorganisms. |
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| NETs |
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| What is programmed cell death? |
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| Apoptosis |
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| What is cell death following an injury? |
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| Necrosis |
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| The presence of phosphatidylserine in the outer leaflet does what? |
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| 1. Helps signal nearby cells and macrophages to phagocytose the apoptotic cell. "Eat Me" signal 2. Blocks inflammation, inhibits the production of inflammation-inducing signals (cytokines) by the phagocytic cell |
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| Apotpsis depends on an intracellular proteolytic cascade. Which in turn depends on a family of proteases called? |
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| Caspases |
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| Caspases are synthesized as ____ precursors which are activated by ____ cleavage. |
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| inactive, proteolytic |
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| What cleave and activate other executioner procaspases, as well as specific target proteins in the cells? |
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| Executioner caspases |
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| What pathway involves extracellular signals that bind to cell-surface receptors? |
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| Extrinsic pathway |
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| What are the 3 domains of the death receptors? |
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| 1. Extracellular ligand-binding domain 2. Single transmembrane domain 3. Intracellular "death" domain |
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| What has a ligand binding domain but not a death domain. It also competitively inhibits the death receptors? |
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| Decoy Domain |
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| What resembles an initiator procaspase, but lacks the proteolytic domain. They also compete with initiator procaspases? |
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| Intracellular Blocking Proteins (FLIP) |
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| What is activated in response to injury or other stress, and depends on the mitochondria. |
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| Intrinsic Pathway |
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| What family of proteins mediate and regulate mitochondrial outer membrane permeabilization (MOMP) and apoptosis? |
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| Bcl-2 |
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| What two things are essential for MOMP, and directly cause the membrane disruption? |
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| Bax and Bak |
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| What is the only protein that provides the crucial link between apoptotic stimuli and the intrinsic pathway of apoptosis? |
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| BH3 |
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| What block caspases? |
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| IAPs (inhibitors of apoptosis proteins0 |
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| As executioner caspases can activate each other (amplification), they must.... |
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| have mechanisms to limit potential "accidental" activation |
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| Where are IAPs located and what happens when they bind? |
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| Cytosol, they inhibit any spontaneously activated caspases |
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| The cancer forming process is called? |
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| Oncogenesis or tumorigenesis |
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| Cancer causing mutations usually occur in what? |
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| somatic cells |
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| Certain ____ ____ carried in the germ line increase the probability that cancer will occur at some time. |
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| inherited mutations |
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| What are the 6 ways tumor cells differ from normal cells? |
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| 1. Drive to proliferate 2. Insensitivity to anitgrowth signals 3. Evasion of apoptosis 4. Tissue invasion 5. Angiogenesis 6. Self-sufficiency in growth signals |
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| What tumors derive from epithelia? (lung, breast, stomach) |
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| Carcinomas |
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| What tumors derive from mesenchymal tissues? (bone, cartilage, fat) |
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| Sarcomas |
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| What tumors that start in the cells of the immune system? |
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| Lymphomas |
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| Problems with benign tumors arise if their ____ interferes with normal function of if they ____ ____ |
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| size, secrete hormones |
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| What is the term that describes how tumor cells spread? |
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| Metastasis |
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| What is used by cancer cells to penetrate the ECM? |
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| invadopodium |
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| Malignant cells usually exhibit the characteristics of? |
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| Rapidly growing cells |
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| How do tumors arise from stem cells? |
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| The cells keep dividing and when a mutation occurs they start to accumulate. Then they could turn into cancer cells |
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| As more progenitor cells are made from stem cells what trend do they follow? |
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| As they increase their degree of differentiation, they start to decline in their replication potential. |
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| What are the 4 ways that cancer can occur as the result of changes in behavior of stem cells? |
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| 1. Niche expansion 2. Niche invasion 3. Niche independence 4. Progenitor self renewal |
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| Tumors often arise at sites of ____ or ____ |
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| Injury or infection |
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| Whats expression is induced by low oxygen? |
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| VEGF |
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| What induces transcription of VEGF and is activated by low oxygen? |
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| HIF-1 |
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| What is the term to describe the time when cells can no longer divide? |
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| senescence |
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| Is APC a proto-oncogene or tumor suppressor? |
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| Tumor suppressor because you need a loss of function to get the mutant phenotype |
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| When DNA is damaged what prevents the cell from going from G1 to S phase? |
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| p53 |
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| Activation of p53 can lead to ____ |
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| Apoptosis |
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| What are the 4 ways a proto-oncogene gets converted to a oncogene. |
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| 1. Mutation 2. Amplification 3. Chromosomal translocation (fusion making a chimeric protein) 4. Chromosomal translocation (expression by a different promoter that causes misexpression) |
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| What is a dominant oncogene where the glycine at position 12 changed to another amino acid? |
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| Ras |
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| Ras reduces its GTPas activity and keeps in in the ___ GTP bound state. |
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| active |
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| What promotes cell survival or proliferation, has dominant mutations, arise from point mutations, and cause a gain of function that allows for unregulated cell proliferation and survival? |
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| proto-oncogenes |
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| What normally inhibits cell survival and proliferation, mutations are recessive, arises from deletions and point mutations, and causes a loss of function that allows unregulated cell proliferation and survival? |
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| Tumor-suppressor genes |
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| What normally repairs are prevents DNA damage, mutations are recessive, arises by deletion and point mutations, and causes a loss of function that allows mutations to accumulate? |
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| Caretaker genes |
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| What when mutated allows for the degradation of beta-catenin and thus leads to the activation of proto-oncogenes? |
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| APC |
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| What represses ras? |
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| NF-1 |
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| What activates ras? |
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| Sar and Abl |
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| How does ras cause lead to and increase in cancer? |
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| It reduces the GTPase activity and keeps it in the active GTP bound state. |
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| What adds OH groups to molecules that turns normally harmless molecules to cause damage to DNA? |
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| Cytochrome P-450 |
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| What forms when amino acids and creatine react at high temperatures? |
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| Heterocyclic amines (HCAs) which are carcinogens |
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| What disease causes a disruption in nucleotide repair, which means DNA repair stops functioning properly? |
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| XP |
